Objective: To investigate the impact of brain death (BD) on the morphology and function of liver.
Methods: Fifteen Ba-ma minipigs were randomly divided into 3 equal groups: brain death group (Group B) made into BD models by increasing the intracranial pressure; breviscapine pretreatment group (Group P), with breviscapine 2.5 mg x kg(-1) given intravenous drip 1-2 hours after the successful establishment of BD model; and control group (Group C) undergoing operation similar to that in Group B but without increasing the intracranial pressure. 3, 6, 12, 18, and 24 hours after the initial confirmation of BD blood samples were collected from the superior vena cava to detect the serum alanine transaminase (ALT), aspartate transaminase (AST), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, and a piece of liver tissues were collected to undergo light microscopy and electron microscopy, and immunohistochemistry to examine the expression of protein kinase (PKC)-alpha by RT-PCR.
Results: The levels of serum ALT and AST of Group B began to increase since 12 h after BD, and were both significantly higher than those of Group C 18 and 24 hours after BD (both P < 0.05). The levels of serum ALT and AST of Group P began to increase since 12 h after BD, and were both significantly lower than those of Group B (both P < 0.05). The levels of serum TNF-alpha, IL-1beta, and IL-6 of Group B and Group P began to increase gradually since 3 h after BD, however, those of Group B were all significantly higher than those of group P (all P < 0.05). PKC-alpha was only expressed in the plasma of a few normal liver cells. The PKC-alpha mRNA and protein levels of Groups B and P began to increase since 6 h after BD, however, those of Group B were all significantly higher than those of Group P (all P < 0.05). Light and electron microscopy showed that only mild edema of liver cells was seen in Group P, and since 12 h after BD swelling of mitochondria, edema of liver cells, etc. were seen in Group B, and the morphologic damages were more severe in Group B.
Conclusion: Brain death evokes hepatic functional and morphological injuries. PKC-alpha may involve in the mechanism. Breviscapine inhibits the activation of PKC-alpha, thus reducing the damage in liver.